Mycotoxins are a group of structurally diverse, mold elaborated compounds that induce diseases known as mycotoxicosis in humans and animals. As much as twenty-five percent of the world's food crops are estimated to be contaminated with mycotoxins. Ingestion of sufficient quantities of mycotoxin-contaminated material leads to acute, and more commonly, chronic intoxication. As secondary mold metabolites, mycotoxins may contaminate animal feeds and human food ingredients in the absence of intact fungal elements. In many instances, processing of feed stuff may mask the presence of mold growth without concomitant destruction of mycotoxins. Mycotoxin-contaminated animal feeds and human foods are consumed worldwide, although their adverse health effects are not fully recognized. When a mycotoxicosis occurs in animals, it affects their health and reduces production efficiency because of increased susceptibility to infectious agents as a result of immune suppression. This has grave economic consequences. Furthermore, ingestion of such animals may have subtle health effects on humans which are not currently understood.
Although it is known that fungi are capable of producing mycotoxins that frequently contaminate the food consumed by humans and animals, precise factors that initiate mycotoxin production are not well defined. The exact type and extent of the mycotoxin contamination is a function of mold types, growth conditions during the crop season, and storage practices. Mycotoxins of major concern include aflatoxin, zearalenone, fumonosin, ochratoxin, vomitoxin, etc.
Aflatoxins are a group of potent liver toxins produced mainly by strains of Aspergillus flavus and Aspergillus parasiticus, which coexist with and grow on almost any crop or food. They are designated as aflatoxin B.sub.1, B.sub.2, G.sub.1, G.sub.2, M.sub.1, etc. The most abundant and toxic member of aflatoxins under natural contamination is aflatoxin B.sub.1, which is one of the most potent known hepatocarcinogens. Aflatoxins depress carbohydrate metabolism, decrease protein synthesis, impair lipid transport and key enzyme systems, and reduce natural defense mechanisms in animals. Generally, young animals are more susceptible to the toxic effects than mature animals. Poultry are more sensitive to the adverse effects of aflatoxins than mammals. Among domestic mammals, the approximate order of sensitivity from most to least is: dogs&gt;young swine&gt;pregnant sows&gt;calves&gt;fattening pigs&gt;mature cattle&gt;sheep. The relative resistance of mature ruminants is a result of rumen detoxification mechanisms.
Clinical aflatoxicosis is primarily a reflection of liver dysfunction. Subacute aflatoxicosis in swine is characterized by decreased feed conversion efficiency, depressed growth, toxic hepatitis, ictus, toxic nephritis, and hemorrhage enteritis. Daily exposure to aflatoxin for more than 7-10 days results in liver lesions of fibrosis, edema of the gall bladder, centrilobular hemorrhage, fatty change, cnecrosis, and biliary hyperplasia. In swine rations, dietary levels of 2-4 ppm aflatoxin lead to acute fatal toxicosis while rations containing 260 ppb for several weeks cause reduced growth rate. A protein-deficient diet enhances the toxicity of aflatoxin, while a high protein diet is somewhat ameliorating. There is extensive evidence that aflatoxin depresses cell mediated immune function, thus lowering the resistance of several animal species to bacterial, fungal and parasitic infections.
Cattle, sheep, and other ruminants appear less susceptible to aflatoxin than monogastric mammals or poultry. Calves, which are functionally monogastrics, are more susceptible than mature cattle. Generally, rations containing 1-2 ppm aflatoxin fed to mature cattle for a few weeks result in reduced weight gain and depressed milk production. Rations with as little as 1 ppm aflatoxin are lethal to steers within 60 days. Aflatoxicosis in cattle is mainly manifested by symptoms such as depression, anorexia, reduced growth, decreased milk production, subnormal body temperature and dry muzzle. As in several other species, lesions in the liver include fatty degeneration, vacuolated liver cells, liver necrosis, bile duct proliferation, and diffuse fibrosis.
Zearalenone is another mycotoxin of concern. It is a resorcyclic lactone produced primarily by fusarium roseum. This mycotoxin has been detected in corn, wheat, barley, oats, sorghum, rice, sesame, commercial rations, corn silage, corn meal and corn flakes. Zearalenone induces estrogenic effects in many species. Organs normally receptive to estrogenic compounds include tabular organs of female reproductive tract, ovaries, and mammae. Prepubertal female swine are most sensitive to zearalenone. They may ultimately develop rectal and vaginal prolapses. Other reported problems in female swine include anestrus, contraception failure, pseudopregnancy, decreased pigs per litter, and abortion. Zearalenone also induces feminization in immature male swine characterized by testicular atrophy, swelling of the prepuse and mammary glands. Mature male swine are highly resistant to the effects of zearalenone. Unusually high concentrations of zearalenone in cattle rations lead to infertility and udder enlargement.
In an effort to minimize the effect of mycotoxin-contaminated food supplies, numerous methods have been developed to control the formation of mycotoxins, to detoxify, or to decontaminate the contaminated foodstuff. Traditional methods of dealing with grains contaminated with mycotoxins are: blending a contaminated grain with a clean grain to reduce the contamination level, screening or using other means of physical separation to remove the highly contaminated grain, and ammoniation or heating to detoxify the contaminated grain. Although ammoniation of animal feeds results in a significant degradation of aflatoxins in peanuts, corn seed meals, and corn, the economic liability of ammoniation precludes it from practical applications.
In the meantime, various clays have been used as aflatoxin binders in animal feeds. For example, a montmorillonite clay mixed with a mycotoxin-contaminated animal feed was fed to animals to increase the nutritional value of the feed. Similarly, an acid-activated calcium bentonite clay mixed with a contaminated feed was fed to an animal to increase weight gain of the animal. In addition, a phyllosilicate material was also found to be capable of inactivating mycotoxins in an animal feed.
Although these methods achieved varying degree of success in reducing adverse effects of a single mycotoxin, they are generally not effective against a group of mycotoxins such as aflatoxin, fumonosin, ochratoxin, zearalenone, and the like. Because some or all of the mycotoxins frequently contaminate animal feeds, there is a need for a method and a animal feed composition which is effective in decreasing adverse effects of some or all of the mycotoxins, thereby promoting weight gain in animals.